1;Preface to the Fifth Edition;6 2;Contents;7 3;1: Historical Aspects;12 3.1;1.1 Introduction;12 3.2;1.2 Historical Aspects of Patch Testing;13 3.2.1;1.2.1 The Pre-Jadassohn Period;13 3.2.2;1.2.2 Josef Jadassohn, the Father of Patch Testing in Dermatology;13 3.2.3;1.2.3 Jean-Henri Fabre's Experiments;14 3.2.4;1.2.4 A General Overview of Patch Testing During the Period 1895-1965;15 3.2.5;1.2.5 Bruno Bloch's Pioneering Work in Basel and in Zurich;15 3.2.6;1.2.6 The Influence of Poul Bonnevie in Scandinavian Countries;16 3.2.7;1.2.7 A Controversial Period: The Pros and Cons of a Standard Series;17 3.2.8;1.2.8 Marion Sulzberger, the Initiator of Patch Testing in North America and Alexander Fisher, a World Leader in the Field of C;17 3.2.9;1.2.9 The Founding of Groups;17 3.2.10;1.2.10 The Founding of the European Environmental and Contact Dermatitis Research Group (EECDRG) and the European Society of Co;18 3.2.11;1.2.11 Dermatochemistry and Contact Dermatitis;18 3.2.12;1.2.12 Recent Advances in the Management of Patch Testing;18 3.3;1.3 Historical Aspects of Prick Testing;19 3.4;References;19 4;Part 1: Basic Features;21 4.1;2: Genetics and Individual Predispositions in Contact Dermatitis;22 4.1.1;2.1 General Introduction;23 4.1.2;2.2 Genetic Factors in Allergic Contact Dermatitis1;23 4.1.2.1;2.2.1 Early Studies in the Genetics of Contact Allergy;24 4.1.2.1.1;2.2.1.1 Experimental Sensitization;24 4.1.2.1.2;2.2.1.2 Family Studies;25 4.1.2.1.3;2.2.1.3 Twin Studies;25 4.1.2.1.4;2.2.1.4 Studies of Immunogenetic Markers;26 4.1.2.2;2.2.2 In Search of the Phenotype of Contact Allergy: Polysensitization;26 4.1.2.3;2.2.3 Polymorphisms in Allergic Contact Dermatitis;27 4.1.2.3.1;2.2.3.1 Tumor Necrosis Factor (TNF);28 4.1.2.3.1.1;Studies of TNF Polymorphisms in ACD (See Table 2.4);28 4.1.2.3.2;2.2.3.2 Interleukin-16;31 4.1.2.3.2.1;Studies of IL-16 Polymorphisms in ACD;31 4.1.2.3.3;2.2.3.3 N-Acetyltransferase 1 and 2 (NAT1/NAT2);31 4.1.2.3.3.1;Studies of NAT: Polymorphisms in ACD;32 4.1.2.3.4;2.2.3.4 Glutathione Transferases M1 and T1 (GSTM1 and GSTT1);33 4.1.2.3.4.1;Studies of GSTM1 and GSTT1 Polymorphisms in ACD;34 4.1.2.3.5;2.2.3.5 Manganese Superoxide Dismutase;34 4.1.2.3.5.1;Studies of the MnSOD Polymorphisms in ACD;34 4.1.2.3.6;2.2.3.6 Angiotensin-Converting Enzyme;35 4.1.2.3.6.1;Studies of the ACE Polymorphisms in ACD;35 4.1.2.3.7;2.2.3.7 Filaggrin;35 4.1.2.3.7.1;Studies of FLG Mutations in ACD;35 4.1.2.3.8;2.2.3.8 General Remarks on the Study of "Candidate Gene" Polymorphisms in ACD;36 4.1.3;2.3 Irritant Contact Dermatitis;37 4.1.3.1;2.3.1 Individual Variability in Irritant Responses in Healthy Individuals;38 4.1.3.2;2.3.2 Predisposition Related to Specific Phenotypes;39 4.1.3.2.1;2.3.2.1 Atopic Dermatitis;39 4.1.3.2.2;2.3.2.2 Sex;40 4.1.3.2.3;2.3.2.3 Age;40 4.1.3.2.4;2.3.2.4 Ethnicity;40 4.1.3.2.5;2.3.2.5 Other Skin Diseases;41 4.1.3.2.6;2.3.2.6 Regional Differences;41 4.1.3.2.7;2.3.2.7 Skin Type;41 4.1.3.2.8;2.3.2.8 Body Mass Index;41 4.1.3.3;2.3.3 Genetic Predisposing Factors;42 4.1.4;References;43 4.2;3: Mechanisms of Irritant and Allergic Contact Dermatitis;52 4.2.1;3.1 Introduction;52 4.2.2;3.2 Irritant Contact Dermatitis;52 4.2.2.1;3.2.1 Skin Barrier Perturbation Can Lead to Irritant Contact Dermatitis;52 4.2.2.2;3.2.2 Pathogenesis of Acute Irritant Contact Dermatitis;53 4.2.2.3;3.2.3 Development of Chronic Irritant Contact Dermatitis;55 4.2.2.4;3.2.4 Genetic Risk Factors in Irritant Contact Dermatitis and Atopic Dermatitis;56 4.2.2.5;3.2.5 Cellular Immunological Changes in Irritant Contact Dermatitis;56 4.2.3;3.3 Introduction Allergic Contact Dermatitis;57 4.2.3.1;3.3.1 Binding of Contact Allergens to Skin Components;59 4.2.3.1.1;3.3.1.1 Chemical Nature of Contact Allergens;59 4.2.3.1.2;3.3.1.2 Hapten Presentation by Langerhans Cells (LC);60 4.2.3.1.3;3.3.1.3 Pre and Prohaptens;60 4.2.3.2;3.3.2 Hapten-Induced Activation of Allergen-Presenting Cells;61 4.2.3.2.1;3.3.2.1 Physiology of Langerhans Cells;61 4.2.3.2.2;3.3.2.2 Hapten-I